• Arnoldo Santos, Eva Gomez-Peñalver, M Ignacio Monge-Garcia, Jaime Retamal, João Batista Borges, Gerardo Tusman, Goran Hedenstierna, Anders Larsson, and Fernando Suarez-Sipmann.
• 1Hedenstierna Laboratory, Department of Surgical Sciences, Section of Anaesthesiology & Critical Care, Uppsala University, Uppsala, Sweden. 2CIBER de enfermedades respiratorias (CIBERES), Madrid, Spain. 3Centro Nacional de Investigaciones Cardiovasculares Carlos III, CNIC, Madrid, Spain. 4Intensive Care Unit, Hospital General de Villalba, Villalba, Spain. 5Intensive Care Unit, Hospital del SAS, Jerez de la Frontera, Spain. 6Departamento de Medicina Intensiva, Pontificia Universidad Católica de Chile, Santiago, Chile. 7Division of Pulmonary, Heart Institute (InCor), Hospital das Clinicas, University of São Paulo, São Paulo, Brazil. 8Department of Anesthesia, Hospital Privado de Comunidad, Mar del Plata, Argentina. 9Department of Medical Sciences, Clinical Physiology, Uppsala University, Uppsala, Sweden.
• Crit. Care Med. 2017 Nov 1; 45 (11): e1157-e1164.

ObjectivesTo compare the effects of two lung-protective ventilation strategies on pulmonary vascular mechanics in early acute respiratory distress syndrome.DesignExperimental study.SettingUniversity animal research laboratory.SubjectsTwelve pigs (30.8 ± 2.5 kg).InterventionsAcute respiratory distress syndrome was induced by repeated lung lavages and injurious mechanical ventilation. Thereafter, animals were randomized to 4 hours ventilation according to the Acute Respiratory Distress Syndrome Network protocol or to an open lung approach strategy. Pressure and flow sensors placed at the pulmonary artery trunk allowed continuous assessment of pulmonary artery resistance, effective elastance, compliance, and reflected pressure waves. Respiratory mechanics and gas exchange data were collected.Measurements And Main ResultsAcute respiratory distress syndrome led to pulmonary vascular mechanics deterioration. Four hours after randomization, pulmonary vascular mechanics was similar in Acute Respiratory Distress Syndrome Network and open lung approach: resistance (578 ± 252 vs 626 ± 153 dyn.s/cm; p = 0.714), effective elastance, (0.63 ± 0.22 vs 0.58 ± 0.17 mm Hg/mL; p = 0.710), compliance (1.19 ± 0.8 vs 1.50 ± 0.27 mL/mm Hg; p = 0.437), and reflection index (0.36 ± 0.04 vs 0.34 ± 0.09; p = 0.680). Open lung approach as compared to Acute Respiratory Distress Syndrome Network was associated with improved dynamic respiratory compliance (17.3 ± 2.6 vs 10.5 ± 1.3 mL/cm H2O; p < 0.001), driving pressure (9.6 ± 1.3 vs 19.3 ± 2.7 cm H2O; p < 0.001), and venous admixture (0.05 ± 0.01 vs 0.22 ± 0.03, p < 0.001) and lower mean pulmonary artery pressure (26 ± 3 vs 34 ± 7 mm Hg; p = 0.045) despite of using a higher positive end-expiratory pressure (17.4 ± 0.7 vs 9.5 ± 2.4 cm H2O; p < 0.001). Cardiac index, however, was lower in open lung approach (1.42 ± 0.16 vs 2.27 ± 0.48 L/min; p = 0.005).ConclusionsIn this experimental model, Acute Respiratory Distress Syndrome Network and open lung approach affected pulmonary vascular mechanics similarly. The use of higher positive end-expiratory pressures in the open lung approach strategy did not worsen pulmonary vascular mechanics, improved lung mechanics, and gas exchange but at the expense of a lower cardiac index.

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